LAUSR

UPDRS-III with dyskinesia (Supporting Information Table S1). However, she developed FOG on gait initiation, straight walking, doorways, and turning. FOG was associated with rising up onto the toes during straight walking and onto the toe of the outer rotating foot when turning, raising the possibility of a dystonic phenomenon (Video 2). She was diagnosed with on-state FOG. L-dopa was changed to immediate release and fractionated, amantadine 200 mg daily added, and she commenced gait rehabilitation without improvement. Intermittent subcutaneous apomorphine injections were initiated; however, after 6 months’ therapy, FOG severity was increased (Fig. 1), leading to ~20 falls a day. Based on previous observations, she commenced a 16-hour LCIG infusion. During week 1 of LCIG titration, FOG persisted despite rates that improved parkinsonism while causing dyskinesia, reaffirming on-state FOG. We then performed a rapid infusion titration with hourly increments in the continuous rate of 0.1 to 0.2 mL over 5 hours, starting from 2.1 mL/h, and discovered a higher rate of 3.0 mL/h that led to near-complete resolution of FOG. At 6 months, FOG remained much improved with ≤1 fall per week; however, she still reported FOG when using LCIG extra doses. At 7 months, she converted to 24-hour LCIG with a nocturnal rate of 1.4 mL/h for treatment of nocturnal left foot dystonia. Nocturnal oral L-dopa was no longer required. She reduced her daytime rate from 3.0 to 2.9 mL/h. At 9 months (Video 3), FOG was further reduced, averaging 1 fall every 4 weeks. Pre-LCIG, she had used a wheelchair intermittently for 6 months. She now always walks without aids and no longer avoids escalators or misses lift doors. She experiences two to three occurrences of start hesitation daily and mild, nondisabling dyskinesia of the right leg. Extra doses for mild, nondisabling off periods sometimes trigger transient start hesitation. Hand function is excellent and she recently resumed playing piano. We explored LCIG as treatment for on-state FOG because plasma L-dopa levels with an LCIG infusion are more predictable than oral L-dopa dosing. We surprisingly discovered an interaction between L-dopa infusion rates and FOG behavior that suggested the existence of another FOG subtype (Fig. 1). We suggest the term “triphasic-on” FOG, to denote its presence in both “on” and “supra-on” states, but also the presence of a narrow “on” therapeutic window in the transition between these two states where FOG improves. It is plausible that “triphasic-on” FOG may have been present, but obscured, in at least some of the patients reported on by Espay and colleagues because of the use of a single supra-on challenge dose and the unpredictable plasma L-dopa levels following oral L-dopa. In conclusion, our case suggests that some PD patients with on-state FOG might be able to be treated successfully and implies the existence of additional FOG subtypes.